Avian erythrocytes extrude substantial quantities of cyclic AMP in response to beta-adrenergic stimulation. This extrusion depends on metabolic energy, seems distinct from the enzymes that produce and degrade cyclic AMP, is inhibited by prostaglandins (especially PGA1) and is quite sensitive to changes in temperature (no extrusion occurs below 22 degrees C). We plan to describe this efflux mechanistically by classical kinetic studies and to assess the contribution to cyclic AMP efflux of other transport systems. We will study the interaction of PGA1 effect. To understand the effects of temperature and PGA1 on membrane properties, we will study their effects on membrane fluidity by estimating membrane viscosity by fluorescence depolarization. We will also consider the role of membrane bound protein kinases and the phosphorylation of membrane substrates in cyclic AMP extrusion, using S49 lymphoma cells (with a variant lacking protein kinase). We will attempt to identify components of cyclic AMP transport by photo-affinity labelling using radioactive 8-azido-cyclic AMP. We have also extended these studies to mammalian reticulocytes, an ontogenetically useful system.